Global Cerebral Edema After Subarachnoid Hemorrhage

Abstract

Background and Purpose-Cerebral edema visualized by CT is often seen after subarachnoid hemorrhage (SAH).Inflammatory or circulatory mechanisms have been postulated to explain this radiographic observation after SAH. We sought to determine the frequency, causes, and impact on outcome of early and delayed global cerebral edema after SAH. Methods-We evaluated the presence of global edema on admission and follow-up CT scans in 374 SAH patients admitted within 5 days of onset to our Neurological Intensive Care Unit between July 1996 and February 2001. Using multivariate analysis, we identified predictors of global cerebral edema and evaluated the impact of global edema on outcome 3 months after onset with the modified Rankin Scale. Results-Global edema was present on admission CT scans in 8% (nϭ29) and developed secondarily in 12% (nϭ44) of the patients. Global edema on admission was predicted by loss of consciousness at ictus and increasing Hunt-Hess grade. Delayed global edema was predicted by aneurysm size Ͼ10 mm, loss of consciousness at ictus, use of vasopressors, and increased SAH sum scores. Thirty-seven percent (nϭ137) of the patients were dead or severely disabled (modified Rankin Scale 4 to 6) at 3 months. Death or severe disability was predicted by any global edema, aneurysm size Ͼ10 mm, loss of consciousness at ictus, increased National Institutes of Health Stroke Scale scores, and older age. Conclusions-Global edema is an independent risk factor for mortality and poor outcome after SAH. Loss of consciousness, which may reflect ictal cerebral circulatory arrest, is a risk factor for admission global edema, and vasopressor-induced hypertension is associated with the development of delayed global edema. Critical care management strategies that minimize edema formation after SAH may improve outcome.

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

“…Patients with cerebral edema develop cerebral hypermetabolism (Zetterling et al., 2010), which may increase the energy demand in the brain. Hypermetabolism is linked to disability and cognitive dysfunction (Claassen et al., 2002). Previous studies have demonstrated that white matter (WM) hyperintensity is associated with muscle function (Kilgour, Todd, & Starr, 2014) and that docosahexaenoic acid improves short‐ and long‐term neurological performance as well as reduces cerebral edema (Schober et al., 2016).…”

Management of raised intracranial pressure in aneurysmal subarachnoid hemorrhage: time for a consensus?

“…34,51,74 Elevated ICP and its etiologies (ICH, IVH, global edema, and so on) have all been found to be independent predictors of death. 13,53,62,71 While this association has been identified in large retrospective series, the impact of high ICP on aSAH outcomes has not yet been evaluated in large prospective multicenter series. However, a recent systematic review that examined 26 studies focusing on elevated ICP and aSAH outcomes also concluded that higher ICP following aSAH was associated with a higher mortality rate.…”

“…The population was composed of poor-grade patients. A second study by Bentsen et al 5 in Diffuse injury/edema (without mass lesions) occurs in less than 10% of aSAH patients and is not a common indication for DC in aSAH 13,29 "Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg body weight"…”

“…13 It can be seen on initial CT scans after aneurysm rupture in 8% of patients but may also be found in delayed fashion in 10%-12% of patients. 13 The pathophysiology of global cerebral edema is complex and the postulated mechanisms involved include intracranial circulatory arrest and sudden increase in ICP.…”

“…13 It can be seen on initial CT scans after aneurysm rupture in 8% of patients but may also be found in delayed fashion in 10%-12% of patients. 13 The pathophysiology of global cerebral edema is complex and the postulated mechanisms involved include intracranial circulatory arrest and sudden increase in ICP. 53 Severe refractory vasospasm is not uncommon following aSAH and may require aggressive treatment with intraarterial vasodilator therapy using nicardipine, papaverine, milrinone, verapamil, or a combination of those.…”